A contract research project was conducted to compare the toxicity and bioavailability of lead oxide, lead sulfide, lead acetate, and a sample of lead ore concentrate from Alaska. The chemicals were fed to rats for 30 days at doses of 10, 30, and 100 ppm. The comparative bioavailability of the different types of lead materials were evaluated by measuring the accumulation of lead in the blood and bone. Urinary aminolevulinic acid was determined as a measure of lead toxicity that could be compared to lead-induced elevations of aminolevulinic acid reported in human urine samples. Lead from lead acetate and lead oxide accumulated rapidly in a dose-related fashion in the bone, such that peak concentrations of 200-30O micro-g/gm were attained in the 100 ppm dose group. A steady, dose-related, but much slower rate of accumulation of lead from lead sulfide and the Alaskan lead concentrate sample occurred in the bone, such that peak concentrations of 10-15 micro-g/gm were attained. There was a strong correlation between the elevations in bone lead and that of urinary aminolevulinic acid in rats fed the soluble lead acetate and lead oxide salts, but no correlation in rats fed the insoluble lead sulfide and the Alaskan lead concentrate. There was no elevation of urinary aminolevulinic acid in the latter animals, indicating accumulation of bone lead concentrations >15 pg/gm were necessary before inhibition of a marker enzyme for lead toxicity, aminolevulinic acid dehydratase, would result in excess excretion of urinary aminolevulinic acid. Analyses of lead in serial samples of blood, as well as evaluation of histopathology in the bone, kidney, liver, and brain are in progress. In addition, samples of selected target organs were archived from the study for potential future investigations on lead toxicity.